Tagged: treatment

It is one of the most frequent non-motor features of Parkinson’s and yet it is one of the least publicly discussed.

The word ‘constipation’ is generally used to describe bowel movements that are infrequent or difficult to pass. The stool is often dry, lumpy and hard, and problematic to expel. Other symptoms can include abdominal pain, bloating, and the feeling that one has not completely passed the bowel movement.

In today’s post we look at what can cause constipation, why it may be so common in Parkinson’s, discuss what can be done to alleviate it, and look at clinical trials focused on this issue.

As many as 1 in 5 people say they have suffered from chronic (long-term) constipation at some point in their lives.

It results in more than 2.5 million hospital and physicians visits per year in the USA.

And Americans spend more than $700 million on treatments for it annually (Source).

More importantly, constipation is considered by many researchers to be a risk factor for developing Parkinson’s, as many people in the affected community claim to have experienced constipation for long periods prior to diagnosis.

Why this is, what is being done to research it, and what can be done about constipation in Parkinson’s is the topic of today’s post. But first, let’s start with the obvious question:

Regular readers will be aware that here at the SoPD, we are on a mission to change the way we clinically test drugs (Click here for the most recent rant on this topic).

We have a lot of interesting drugs waiting in the pipeline to be clinically tested and an eager (read: desperate) population of individuals affected by Parkinson’s, but we are missing one critical part of the equation: better tools of assessment.

How can we determine whether a drug is actually working or not? And how can we better monitor people over time on said drug?

Our current methods assessing individuals with Parkinson’s rely heavily on clinical rating scales and brain imaging. These are basic tools at best, conducted episodically (annually in general, or once every 2-6 months during a clinical trial), and provide little in the way of useful objective data (on an individual basis).

In today’s post, we will look at a single aspect of Parkinson’s – sleep – and try to nut-out a better/more informative method of assessing it over time.

In their press release, the company provided the results of a long-term Phase I clinical trial testing the tolerability and safety of their treatment AFFITOPE® PD01A.

The treatment was found to be safe and well-tolerated in people with Parkinson’s. But there was one sentence which was particularly intriguing in the press release regarding clinical symptoms.

In today’s post, we will discuss what is meant by ‘immunotherapy’, outline what this particular clinical trial involved, review the results, and explore what this could mean for the Parkinson’s community.

This week multiple research groups at the University of Oxford and Boston-based FORMA Therapeutics announced a collaboration to identify, validate and develop deubiquitinating enzyme (DUB) inhibitors for the treatment of neurodegenerative conditions, like Parkinson’s.

But what exactly are DUB inhibitors? And how do they work?

In today’s post, we will answer these questions, look at what the new collaboration involves, and look at what else is happening with DUB inhibitors for Parkinson’s.

Dubstep is a genre of electronic dance music that originated in South London in the late 1990s. Only recently -in the 2010s – has the culture really become more mainstream. And while I have a hard time appreciating the heavy bass music (man, I am becoming a grumpy old man before my time), it is amazing to watch some of the dancers who robotically embody this form of music:

The guy on the right is named Marquese Scott. Sometimes he simply defies the laws of physics.

The title of today’s post is a play on words, because rather than doing ‘Dubstep’ we are going to be discussing how to ‘DUB-stop’.

Researchers in Oxford have recently signed an agreement with a US company to focus resources and attention on a new approach for tackling neurodegenerative conditions, including Parkinson’s.

Diagnosed at 46 with Parkinson’s, Mariëtte keeps a great blog that touches on many areas of life, including boxing. But it also provides her with a medium to discuss how she lives with Parkinson’s (you should follow her if you don’t already).

Her answer is ‘Yes!‘ and she listed 10 areas where the differences are apparent.

Mariëtte’s points are made from an educated point of view – she is a very dedicated Parkinson’s research advocate.

Reading through her post, however, I saw it as a nice opportunity to provide the view of things from the other world (Planet Researcher). So, with her permission, I have copied her 10 points here and I have tried to provide a Planet Researcher view of her thoughts (below in red). And I should add that I do not speak for everyone on Planet Researcher – my views are simply that: mine.

In a recent SoPD post, we discussed the importance of calcium and looked at how it interacts with the Parkinson’s-associated protein alpha synuclein, affecting the function and clustering of that protein.

During the writing of that post, another interesting research report was published on the same topic of calcium and alpha synuclein. It involved a different aspect of biology in the cell – a structure called theendoplasmic reticulum – but the findings of that study could also explain some aspects of Parkinson’s.

In today’s post, we will review the new research report, consider the biology behind the findings and how it could relate to Parkinson’s, and discuss how this new information could be used.

I can remember my father often saying “If you kids don’t be quiet, I’ll go berserk!”

Growing up, I never questioned the meaning of the word ‘berserk‘.

I simply took it as defining the state of mindless madness that my dad could potentially enter if we – his off-spring – pushed him a wee bit too far (and for the record, Dad actually ‘going berserk’ was a very rare event).

So, what happened during April 2018?

April 27th – Kim Jong-un crosses into South Korea to meet with President Moon Jae-in, becoming the first North Korean leader to cross the Demilitarised Zone since its creation in 1953. In initial small steps towards reconciliation, South Korea said it would remove loudspeakers that blare propaganda across the border, while North Korea said it would shift its clocks to align with its southern neighbour.

And finally the city of Trier in Germany is already struggling to keep up with demand for ‘0-euro’ notes, bearing the face of its most famous son and communism’s creator Karl Marx. Sold for 3 euros each, the notes are part of celebrations for his 200th birthday (5th May 1818).

The cryptic title of this post will hopefully make sense by the time you have finished reading the material present here.

This week, new research from the USA points towards an increased risk of Parkinson’s (PD) for people that suffer from inflammatory bowel disease (IBD).

That same research, however, also points towards a clinically available treatment that appears to reduce the risk of Parkinson’s in individuals affected by inflammatory bowel disease. That treatment being: anti–tumor necrosis factorantibodies (TNF AB). Is that title making sense yet? If not, read on.

In today’s post, we will outline what inflammatory bowel disease is, review what the new research found, and discuss what is known about TNF in Parkinson’s.

There has been an increased incidence of IBD since World War II, which could be associated with increased awareness and reporting of the condition, but it could also be linked with increases in meat consumption (Click here to read more about this). For example, in 2015, an estimated 1.3% of U.S. adults (3 million) were diagnosed with IBD, which was a large increase on the levels in 1999 (0.9% or 2 million adults – Source: CDC).

This is delightful, but what does it have to do with Parkinson’s?

So this week, an interesting study was published on the Journal of the American Medical Association – Neurology edition website:

Bumetanide (Bumex) is a diuretic drug (a medication that removes water, by increasing the production of urine). It is used to treat swelling caused by heart failure or liver or kidney disease.

Recently, researchers in France have been exploring its use in Parkinson’s, and their results are really interesting.

‘Interesting’ because they not only point towards a clinically available drug that could (potentially) be repurposed for the treatments of Parkinson’s, but they also help to explain how our brains control movement.

In today’s post we will review the new results, discuss what they suggest about our ability to move, and we will look at efforts to take this drug to the clinic for Parkinson’s.

Heart failure (sometimes referred to as congestive heart failure) occurs when the heart is unable to pump sufficiently enough to maintain the required blood flow to meet the body’s needs. The most common causes of heart failure include coronary artery disease, high blood pressure, atrial fibrillation,valvular heart disease, and lifestyle issues (such as excess alcohol use). Overall around 2% of adults have heart failure; in those over the age of 65, this percentage increases to 6–10%. In 2015, it was estimated to affected approximately 40 million people worldwide (Source).

Common symptoms include:

shortness of breath

excessive tiredness

leg swelling.

A common treatment option for heart failure are diuretics.

What are diuretics?

Diuretics (sometimes called water pills) are medications that have been designed to increase the amount of water and salt expelled from the body as urine.

There are three types of diuretic medications. They are:

Thiazide

Loop

Potassium-sparing

Thiazide diuretics are the most commonly prescribed, generally for the treatment of high blood pressure. This class of drugs not only decreases the level of fluids in your body, they also cause your blood vessels to relax. Potassium-sparing diuretics reduce fluid levels in your body without – as the label suggests – causing you to lose potassium. The other types of diuretics can cause you to lose potassium, which can result in other health complications such as arrhythmia.

And then there are loop diuretics, which also decrease the level of fluid in the body.

But some loop diuretics have additional properties. And today we are going to have a look at one of them in the context of Parkinson’s.

A reader recently asked me about an experimental drug called Ibudilast.

It is a ‘Phosphodiesterase 4 inhibitor’.

Recently there was a very interesting result in a clinical trial looking at Ibudilast in a specific neurodegenerative condition. Sadly for the reader that condition was not Parkinson’s, in fact very little research has been done on Ibudilast in Parkinson’s

In today’s post we will look at what Phosphodiesterase inhibitors are, how they work, and discuss why Ibudilast may not be such a good experimental treatment for Parkinson’s.

I will not be at the meeting, but I will definitely be keeping an eye out for any news regarding the results of one particular clinical trial. At the meeting, a biopharmaceutical company called MediciNova Inc. will be presenting data regarding one of theirclinical trials.

Dr Brooks will be presenting the results of a single-center, randomized, double-blind, placebo-controlled clnical trial which was conducted to evaluate the safety, tolerability and clinical endpoint responsiveness of a drug called Ibudilast (or MN-166) in subjects with the neurodegenerative condition, Amyotrophic Lateral Sclerosis (or ALS – also known as motor neuron disease; Click here to read a previous SoPD post about ALS and Click here to learn more about this clinical trial).